Biased Competition Favoring Physical Over Emotional Pain: A Possible Explanation for the Link Between Early Adversity and Chronic Pain.

Abstract

Early adversity predisposes to chronic pain, but a mechanistic explanation is lacking. Survivors of early adversity with chronic pain often seem impaired in their ability to be aware of, understand, and express distressing emotions such as anger and fear in social contexts. In this context, it has been proposed that pain may at times serve as a "psychic regulator" by preventing awareness of more intolerable emotions. This narrative review builds on the premise that physical pain and emotional pain are conscious experiences that can compete for selective attention. We highlight mechanisms whereby the consequences of early adversity may put emotional pain at a competitive disadvantage. A case history, supportive research findings, and an evidence-based neurobiological model are presented. Arising from abuse or neglect in childhood, impairments in the adult capacity to attend to and/or conceptualize the emotional meaning of felt distress may be associated with impaired engagement of the default network and impaired top-down modulation of affective response generation processes. Persistent and poorly conceptualized affective distress may be associated with reduced emotion regulation ability, reduced vagal tone, increased inflammation, and amplified nociceptive signals. Attention to physical pain may be reinforced by the temporary reduction in negative emotions that it causes. These processes jointly promote biased competition favoring attention to physical pain and away from one's own emotions. They may constitute an unintentional analog of the phenomenon of self-injury in patients with borderline personality disorder in whom the intentional infliction of physical pain serves to downregulate intense emotional distress. Attending to, expressing, and understanding previously unacknowledged psychological distress unrelated to pain may facilitate recovery from chronic pain after early adversity. Mechanistic studies that can validate this clinically derived neurobiological hypothesis are urgently needed.